Nitrogen dioxide and carbon monoxide were biggest risk factors.

Action Points

Note that this cohort study of individuals with SLE found an association between air-pollutant levels and disease severity.

Be aware that the multiple-testing that occurred to assess the "lag" of air pollution on disease activity may have inflated the possibility of a positive association where none exists.

Exposure to air pollution in an urban center was associated with disease activity in childhood-onset systemic lupus erythematosus (C-SLE), Brazilian researchers found.

In their study of C-SLE patients living in metropolitan Sao Paulo, exposure to particulate matter, nitrogen dioxide, and carbon monoxide was a risk factor for C-SLE disease activity measured on a standard scale, they reported online in Arthritis Care and Research.

"We note a marked cumulative effect between 12 and 15 days following exposure to particulate matter, after controlling for other risk factors. This study suggests that exposure to air pollution may be an important trigger of inflammation and may aggravate disease activity," according to Elizabeth Fernandes, MD, MS, of the University of Sao Paulo, and colleagues.

Even when atmospheric pollutants are within legally established limits, the authors contended, "they can be harmful to the health of children with SLE."

In large cities, particulate matter is the most harmful vehicular emission to human health, "as it can induce pulmonary inflammation and oxidative stress, which, in turn, may stimulate specific transcription factors such as nuclear factor-K B, activator of protein-1, chemokines, and other serum pro-inflammatory mediators," Fernandes and colleagues added.

Disease activity was measured in 22 C-SLE patients 10 to 19 years old (91% female) from metropolitan Sao Paulo over 409 consecutive medical visits using the Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K). Patients were divided into groups based on SLEDAI ≤8 and SLEDAI >8. Concentrations of particulate matter, sulfur dioxide, nitrogen dioxide, ozone, and carbon monoxide, measured at monitoring stations in various locations around the city on the 31 days preceding the visits, were used to estimate individual exposures.

Daily concentrations of inhaled particular matter, which ranged from 50 mcg/m3 to 100 mcg/m3 over the course of the study, surpassed the standard set by the World Health Organization (WHO) of 50 mcg/m3 on 66 days. These concentrations are considered "unhealthy for sensitive groups" by WHO.

On days with particulate matter levels above the WHO air quality standard of 50 mcg/m3, the risk of C-SLE activity (SLEDAI >8) was increased by 79.0% (95% CI 9.0%-192.0%) compared with days with levels below the standard.

A level of particulate matter in the third tertile, representing >43.92 mcg/m3, increased the risk of SLEDAI-2K >8 by 72.0% (95% CI 7.0%-175.0%) when compared with the first tertile.

In single-pollutant generalized estimation equation models, an increase in the risk of SLEDAI-2K >8 was significantly associated with interquartile ranges of particulate matter (13.4), nitrogen dioxide (25.14 mcg/m3), and carbon monoxide (0.54 ppm) with a lagged effect of 16 days after exposure to particulate matter and 13 days after exposure to nitrogen dioxide and carbon monoxide.

An increase of 13.4 mcg/m3 in the 4-day moving average of particulate matter at a lag time of 12 to 15 days was associated with a 34% increased risk of C-SLE activity (95% CI 7.0%-68.0%). In multiple-pollutants model, none of the pollutants maintained a significant effect on disease activity.

The cumulative effect on SLEDAI-2K in medical visits after 12 to 15 days of exposure to particulate matter "is compatible with a possible time span necessary for inhaled fine and ultrafine particles to trigger and then release vasculoactive molecules and proinflammatory mediators into blood circulation, thus triggering a systemic inflammatory process," the authors wrote.

The lack of an effect of pollutants on disease activity in multiple pollutant models suggests that "the effects that led to C-SLE exacerbation were due to the action of all air pollutants, and that particulate matter may be a possible marker of the complex mixture of air pollutants in the city of Sao Paulo," they add.

Limitations include fixed monitoring stations across the city, which do not fully reflect individual exposure variation. Also, individual data on potential confounders, including exposure to sunlight and cigarette smoke, were not available.

This study was supported by Fundacao de Amparo a Pesquisa do Estado de Sao Paulo, Conselho Nacional de Desenvolvimento Cientifico e Tecnologico, Federico Foundation and Nucleo de Apoio a Pesquisa "Saude da Crianca e do Adolescente" da USP.

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